Abstract
β-amyloid (βA, 39-43 amino acids) deposition in brain parenchyma and vessel walls is a major pathological feature of Alzheimer's disease (AD). This is associated with degenerative changes of neuronal cell bodies and processes, and neuronal death. βA, a portion of a larger transmembrane glycoprotein, has been reported to be toxic in several tissue culture models. The neurotoxic activity of βA synthetic peptides is associated with their fibrillogenic capacity. However, in vivo studies on βA neurotoxic activity have not proved conclusive and further investigations are necessary to establish the pathogenetic role of βA in AD.
Original language | English |
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Pages (from-to) | 211-225 |
Number of pages | 15 |
Journal | Functional Neurology |
Volume | 8 |
Issue number | 3 |
Publication status | Published - 1993 |
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)